i hate med school Flashcards
phenytoin
zero order kinetics
malformation
poor formation of tissue
ex of incomplete morphogenesis
spina bifida
cleft palate
ex of recurrent morphogenesis
having 18 toes (polydactyly)
ear tags
ex of aberrant morphogenesis
ectopic thyroid
deformation + examples of it
unusual forces on normal tissue
club foot
potter sequence (stockings over face disease)
disruption + examples of it
breakdown of normal tissue
digital amputations
vascular accidents that cause ischemia/necrosis
are deformations lethal
rarely
what is a sequence?
when one anomaly triggers a sequence of other anomalies
(spina bifida triggers something downstream, i dont know what)
what does TORCH stand for
T oxoplasmosis
O h no, I have syphillis!
R ubella
C ytomegalovirus
H erpes
memantine
open channel blocker
glutamate NMDA
(for glutamate-gated Ca2+ channel)
tx alzheimers
AMPA/kaitine channel for what NT?
inh or excitatory?
glutamate
excitatory
ondasteron
molec mechanism
what does it treat
5HT3 serotonin blocker
anti emetic after cancer
benzos
allosteric activators of GABA-A
penicillin effect on NT channel
what does it cause?
open channel blocker of GABA-A
causes seizures
strychnine
comp inh of glycine receptor
tetanus toxin
inh glycine release
hyperekplexia
familial startle disease
glycine channels mutated, no inh stimulus
competitive inh
decrease potency, incr EC50
no change in efficacy
non-comp inh
EC50/potency same
decreased efficacy
uncomp inh
decrease efficacy
decr EC50 (incr potency)
ex of receptor that follows constrained subunit model
Nicotinic ACh
ex of receptors that follow sequential change model
ionotropic glutamate receptors
GPCRs
EPSPs/EPPs
activation of NT receptor permeable to Na/Ca causes depolarization
IPSPs
activation of NT receptor permeable to Cl- causes membrane hyperpolarizaiton
what is resting membrane potential established by?
Na/K ATPase
k+ leak channels
describe neuronal action potential + refractory period
for cardiac AP, blocking Na+ channels does what?
blocks upstroke
for cardiac AP, blocking K+ channels does what?
longer AP duration (incr repol time)
for cardiac AP, blocking Ca2+ channels does what?
shorter AP duration (decreased repol time)
terfenadine
off target effect blocked hERG K+ channels –> long QT
people died
sulfonylurea
tx diabetes by binding to and inh KATP channels
what causes KATP channels to close?
what happens when they are closed?
ATP binding, or sulfonylurea binding
causes depol of membrane + opening of Ca2+ channels
vasoconstricition or insulin release
minoxidil
anti HTN
vasodilation
activates & opens KATP channels
tropine/tropium drugs
muscarinic Ach antagonists
increase HR
what histologic change happens during breastfeeding?
lobular hyperplasia
B1 vs B2 effects
one heart (b1) two lungs (b2)
what pathway for growth factors?
RAS/MAPK
(MAPk = mitogen activated protein kinase)
what pathway for insulin?
(RTK)
PI3K/AKT/mTOR
what pathway for cytokines (RTK)
JAK/STAT
explain RTK pathway (general) for RAS/MAPK and PI3K/AKT/mTOR
ligand binds
receptors dimerize
receptors transphosphorylate on Tyr residues
scaffold binds
kinase cascade initiated
explain RTK pathway for JAK STAT
ligand binds STAT
JAK proteins bind and phosphorylate Tyr residues, also serve as scaffold
pSTATs go into nucleus and do things
what do allosteric activators do in regard to receptor desensitization?
decrease likelihood
do ligand channels desensitize
yes, rapidly to orthosteric agonistsf